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Thoracic Surgery

FM Shamji

31-03-2011

Solitary Pulmonary Nodule - SPN

• Also called “coin lesion”• Radiologic diagnosis• Defined as: “Single nodular lesion within the lung

substance, 3 cm or less in diameter, well defined, completely surrounded by normal-appearing lung tissue, not cavitated but may be calcified, usually of clinically undetermined etiology”

• Its importance lies in its diagnosis and a significant number are malignant and resection is followed by good survival rate

• Incidence of malignancy in mass survey varies from 3 to 6%

Classification of Solitary Pulmonary Nodules

1. Neoplasms (45%)Benign

• Hamartoma (most common)• Fibroma• Leiomyoma• Localized fibrous tumor of visceral pleura• Bronchial adenoma

Malignant• Bronchial carcinoma• Carcinoid tumor• Metastases• Lymphoma

Classification of Solitary Pulmonary Nodules

2. Granuloma (40%)

Histoplasmoma

Coccidiodomycoma

Cryptococcoma

Aspergilloma

Tuberculoma

3. Inflammatory (4%)

Lung abscess

Pneumonitis

Rheumatoid nodule

4. Miscellaneous (4%)

Fluid-filled cyst

Infarct

Arteriovenous malformation

Amyloid

Management of Solitary Pulmonary Nodules

Favour Benign Lesion

Well demarcatedDense calcificationUnchanged in size over 2yAbsence of risk factors for

primary lung cancerAbsence of history of

previous malignancy Size < 2cm (not absolute)Young age < 40y (not

absolute)

Favour Malignant Lesion

SpiculatedNot calcifiedProgressive growth over 2yPresence of risk factors for

primary lung cancerHistory of previous

malignancySize > 2cm (not absolute)Older age >40y ( not

absolute)

Investigations for SPN

1. Attempt should be made to find any previous chest films for comparison – present before, same size or getting larger

2. CT scan chest is necessary to search for satellite lesions, enlarged nodes in the mediastinum

3. Percutaneous Fine Needle Aspiration Biopsy is more likely to establish diagnosis than by bronchoscopy

4. PET scan

Asymptomatic RLL Lesion found on routine CXR in 39y man

Questions

• What is a solitary pulmonary nodule?

• What is the differential diagnosis of this lesion?

• Is it necessary to investigate further and how?

Primary Lung Cancer

• Lung cancer is a LETHAL disease

• Has profound effect on society USA each year about 170,000 new cases

and 160,000 die

• Leading cause of cancer-related mortality world-wide over 1.2 million people die of lung cancer each

year

Histological Cell Types

• WHO Committee (1999) pathologic classification into two groups

1. Small cell lung cancer 15 to 20%

2. Non-small cell lung cancer 80 to 85%– Squamous cell carcinoma 25 to 30%– Adenocarcinoma 40 to 50%– Large cell carcinoma 10 to 15%

Etiology and Risk Factors in Lung Cancer

1. TOBACCO (in 85% of the cases)

:8 - to 12 - fold increased risk

:Former smokers remain at an elevated risk for

developing lung cancer even decades after they

stop smoking. 50% of newly diagnosed lung cancer patients are former smokers

:Smoking cessation is vital to reducing rate of lung cancer

:10 years after smoking cessation, risk of lung cancer in former smokers is reduced to ½ of those who continue to smoke

Etiology and Risk Factors in Lung Cancer

2. Environmental Tobacco Smoke (ETS)– Reports in 1981and 1986, non-smoking spouses of

active smokers are 30% more likely to develop lung cancer than those married to non-smokers

3. Asbestos is the first occupational carcinogen recognized to cause lung cancer 1955, as early as 1939– Insulating and fire-proofing

4. Radiation

5. Previous lung disease - pulmonary fibrosis

Etiology and Risk Factors in Lung Cancer

• Radiation– High linear energy transfer (LET) radiation is a risk– Creates ionization in higher tissue density and more

tissue damage– RADON is an inert gas with high LET– Breakdown product in the decay of uranium emitting

alpha particles – affects DNA of respiratory epithelium – Occupational risk factor in Uranium miners– Concern is its presence in indoor air of buildings– Prior treatment of thoracic malignancies (breast,

lymphoma, esophagus) with radiotherapy increases risk for lung cancer

Scarring or fibrosis as a cause of lung cancer

• Lung cancer can develop both in the vicinity of pre-existing localized areas of pulmonary scarring and in patients with more diffuse lung fibrosis

• Microscopic examination of lung scar tissue reveals areas of epithelial hyperplasia associated with unexpected carcinomatous change

• ‘SCAR CANCERS’• Personal smoking history and asbestos exposure in non-

smokers are highly relevant• More adenocarcinoma cell type seen

Occupational causes of lung cancer

Cause Occupation

Asbestos Mining, processing, usage

Radioactivity (radon gas) Metal ore mining, uranium mining,

Fluorspar mining

Nickel Refining

Chromium salts Extraction, production, usage

Arsenic Metal refining, chemical industry, insecticides

Chloro-ethers Organic chemical industry

Mustard gas Manufacture

Volatile coal products Coke oven workers

Printing ink(?) Printing industry

Clinical Presentation - Symptoms GROUP I

Result of investigation of some

new respiratory symptom or

because their pre-existing

respiratory state has worsened

GROUP III

Non-specific symptoms such as

malaise, anorexia, weight loss,

loss of taste for food, fatigue,

depression or recurrent febrile

flu-like illness episodes

GROUP II

No respiratory symptoms at

diagnosis; chance finding of an

opacity on CXR ordered for some

other reason e.g. preoperative,

unrelated complaint – angina,

shoulder discomfort

GROUP IV

Specific Symptoms that are

1.LOCAL - bronchopulmonary

2.From DIRECT intrathoracic

spread OR

3.From SYSTEMIC metastatic spread

Clinical Presentation: Group IV

Specific Symptoms that are directly caused by the lung cancer

1.LOCAL – bronchopulmonary symptoms due to bronchial obstruction – atelectasis - infection, irritation - cough, ulceration - bleeding

2.From DIRECT intrathoracic spread pleura, chest wall, ribs, thoracic spine, SVC, recurrent

laryngeal nerve, mediastinal lymph nodes, pericardium, diaphragm, sympathetic chain at the apex

3.From SYSTEMIC spread – metastases to bone, brain, liver, adrenal glands

Group 4: Symptoms from Systemic Metastasis

• Lung cancer may already have spread to distant sites at initial presentation – Stage IV

• Four most common sites of systemic spread are– Brain, Bone, Liver, and Adrenal gland

• BRAIN metastasis – headaches, nausea, fatigue, motor weakness, seizures, visual change, ataxia, or personality change

• BONE metastasis – continuous pain, pathological fracture, epidural spinal cord compression

• Liver metastasis – nausea, vomiting, cachexia• Adrenals – often asymptomatic, lumbar pain

CLINICAL FINDING INTERPRETATION

Marked dyspnea Coexisting COPD

Hoarse voice with bovine cough Left RLN palsy from tumor invasion

Clubbing, HPO lung cancer NSCLC

Horner’s syndrome Pancoast’s apical tumor

Supraclavicular LN enlargement

Inoperable lung cancer

Stridorous respirations Tumor extension into tracheal carina or trachea

Unilateral wheezing and delayed expansion of ipsilateral hemithorax

Almost complete obstruction of a main bronchus

New subcutaneous nodules metastases

SVCO SVC involved by mediastinal LNs or direct invasion

Raised JVP Pericardial effusion due to tumor invasion

Five Types of Paraneoplastic Syndromes

• Manifestations associated with malignancy but not directly related to distant metastasis

• Very common in lung cancer occurring in– 10% of patients with NSCLC– 50% of patients with SCLC

1. ENDOCRINE manifestations (protein hormone) Cushing’s syndrome (SCLC), Syndrome of Inappropriate

Antidiuretic hormone production (SCLC), hypercalcemia (NSCLC – squamous cell), ß –HCG (NSCLC – large

cell)2. HEMATOLOGIC (SCLC and NSCLC)

Hypochromic anemia, Thrombocytosis,

Paraneoplastic Syndromes

3. NEUROLOGIC (SCLC)due to autoimmune reaction to “onconeural” antigen shared by the cancer and nervous system

– Eaton-Lambert myasthenic syndrome– Subacute cerebellar degeneration – cerebellar ataxia– Peripheral neuropathies– Cancer-associated retinopathy

4. MUSCULOSKELETAL (NSCLC)– Digital clubbing– Hypertrophic pulmonary osteoarthropathy

5. DERMATOLOGIC (SCLC)– Acquired tylosis, erythema gyratum repens, triple palm,

acanthosis nigricans

Local Symptoms: Cough and Hemoptysis - cavitating lung cancer

Centrally located symptomatic lung cancer

Presenting Manifestation in Brain: Hemiparesis – abnormal CT/ PET

Patient came to the ER with weakness in the leg and armand persistent headache

Brain metastases – vasogenic edema

MRI done after PET scan

Abnormal radiologic finding in patient with CNS symptoms: personality change and headache

Patient brought to the ER by spouse because of concern about his behaviour

RUL cancer and Brain Metastases

Fine Needle Aspiration Biopsy for peripheral lung cancer

Pancoast (Superior Sulcus) Tumour

• Lung cancer - mass at the extreme apex of the lung

• Pain - in the lower part of shoulder and inner aspect of the arm (C8 and T1)

• Horner’s syndrome – stellate ganglion (T1)

• Hand – weakness and muscle wasting

Pancoast Tumor: Persistent right chest pain right arm

Investigations needed are:CT scan Chest, Abdomen, Head

MRI ThoraxPET scan

FNA biopsyMediastinal LN Biopsy

Investigations are performed for Diagnosis and Staging

1. CHEST RADIOGRAPH is nearly always abnormal – hilar mass, solitary pulmonary nodule, partial or total atelectasis due to bronchial obstruction, pleural effusion, raised paralysed diaphragm, rib destruction, widening of mediastinum, cavitation in the lesion, ‘pneumonia-like’ changes

2. SPUTUM CYTOLOGY positive yield is increased when tumor is centrally situated with increasing size and when it is in lower lobe: positive cytology from single specimen is 40% and increases to 80% with four specimens

Investigations

3. BRONCHOSCOPY is very useful investigationa. providing diagnostic material in centrally

placed tumors – main bronchus or lobar bronchus

b. providing information about inoperability – paralysed vocal cord, definite tracheal involvement, definite carinal involvement,

4. FINE NEEDLE ASPIRATION is very useful for diagnosis in peripherally placed tumors that are beyond bronchoscopic vision

5. Spiral CT scan Chest and Abdomen for diagnosis and staging

5. Non-invasive preoperative staging by PET scan and MRI or CT head

Treatment for NSCLC Stage Intention Treatment

Localized I + II Cure Surgery + CT; add CT to increase cure by 10 – 15%

Loco-Regional

IIIA + IIIB Depends Induction + Surgery

Concurrent CT + RT

CT alone

Metastatic IIIB Pleural + IV

Palliative BSC +/- CT

Treatment for Stage III NSCLC

IIIA Minimal Bulk

Induction CT + Surgery

30%

IIIA Bulky RT + CT 10 – 20 %

IIIB Not surgical

IIIB Pleural Effusion

Not surgical

Small Cell Lung Cancer

• Highly malignant tumor

• Distinct cell type

• Most common lung cancer associated with ectopic hormone production

• Strong relationship to cigarette smoking– >98% found in smokers– Only about 1% occur in non-smokers

• Most chemosensitive and radiosensitive

Investigating and Managing Massive Hemoptysis

Causes of Hemoptysis

1. Pulmonary Disease

a) Infection

Pneumonia, Lung abscess, Bronchiectasis

TB

Mycosis

Aspergilloma

Mucormycosis

b) Neoplasm

Carcinoma, Carcinoid tumor, Endobronchial Metastases – sarcoma, renal cell ca, colon ca

c) COPD

d) Goodpasture’s syndrome

2. Cardiovascular Disease

a) Mitral stenosis

b) Pulmonary Infarction

c) Thoracic aortic Aneurysm

3. Bleeding Diathesis

a) Leukemia

b) Anticoagulation–

Massive Hemoptysis

• Sudden expectoration of large amounts of blood is an alarming development for patients and as well physicians

• Patient is anxious and terrified at the sight of his own blood, and imagines death to be imminent

• Hemoptysis, if copious, may cause SUDDEN DEATH by ASPHYXIATION

Definition: > 600 mls blood expectorated in 24 hours

• Patient may become drowned in his own blood, which is partly coughed out and partly inhaled into all parts of the tracheobronchial tree and lungs Loss of Lung Function

• Respiratory gas exchange deteriorates, sometimes too rapidly, causing death by ASPHYXIATION

Impending Asphyxiation – Blood Clots in the Airway Dead Space

Source of Bleeding

• Cause is almost always bleeding from a ruptured abnormal BRONCHIAL ARTERY

• Susceptible lung parenchymal lesions are– Cavity: usually of tuberculous origin– Bronchiectasis– Lung abscess– Necrotizing pneumonia– Aspergilloma – Centrally located bronchogenic cancer

Common Errors of Clinical Diagnosis and Treatment

• Airway hemorrhage misdiagnosed as SEVERE HEMATEMESIS: patient arrived in the ER c/o of “throwing up” large amounts of blood and was found to be hypotensive. A bleeding peptic ulcer was suspected even though gastroscopy did not confirm the diagnosis. Readmitted after discharge from ER with same symptom.

• Airway hemorrhage misdiagnosed as SEVERE EPISTAXIS and was referred by the ER physician to ENT specialist who performed nasopharyngeal endoscopy and discharged patient home when source of bleeding could not be seen. Severe bleeding recurred within 24 hours.

Common Errors of Clinical Diagnosis and Treatment

• Severe airway hemorrhage correctly diagnosed but NOT managed properly. Respirologist consulted by ER physician. Flexible bronchoscopy performed was unsatisfactory because of active bleeding – it appeared to be coming from right lung from an area of “extrinsic compression” – missing information was previous right thoracoplasty for chronic pulmonary tuberculosis

• Severe airway hemorrhage correctly diagnosed in the ER. Patient was advised by the ER physician to return to home town 400 km away. Hemoptysis continued enroute and arrived in the ER very requiring urgent operation

Life-threatening Airway Hemorrhage

Definition Cause of Death

MASSIVE HEMOPTYSIS Asphyxiation

> 600 mls blood loss in 24 hours

EXSANGUINATING HEMOPTYSIS Both Hypotension and Asphyxiation

> 1000 mls blood loss in 24 hours

> 150 mls blood loss per hour

Definition

• Any hemoptysis should be considered massive when it ceases to be a sign of underlying lung disease and becomes a threat to life in its own right

Volume > 600 ml/24 hr or Volume > 300 ml/expectoration or Impending airway obstruction or Need for transfusion

Serious problem that carries a high mortality rate

Authors Medical Treatment

Surgical Treatment

Conlan

1983

31.8% 17.6%

Crocco

1968

75% 23%

Garzon

1974

75% 18%

Massive hemoptysis and threat of asphyxiation

Gas exchange is impaired by 2 mechanisms

1. Acute Bronchial Obstruction: as little as 150 mls of blood clot can fill the anatomical dead space causing proximal airway obstruction asphyxiation

2. A large volume of blood can flood the entire lobe or lung asphyxiation

We are addicted to Oxygen

Impending Asphyxiation - Airway Dead Space Blood Clots

We are addicted to Oxygen

Etiology of Massive Hemoptysis

• Lung abscess• Bronchiectasis• Necrotizing pneumonia• Aspergilloma• Tuberculosis• Lung Cancer

Literature review of Causes

N=123 patients Number of cases

TB 47

Bronchiectasis 37

Necrotizing pneumonia 11

Lung abscess 6

Lung cancer 6

Bronchovascular fistula 5

Lung fungal infection 4

Miscellaneous 7

Sources of Bleeding

• Rupture of a bronchial artery – most common source– Tuberculous cavity, aspergilloma, lung abscess,

bronchiectasis, lung cancer, necrotizing pneumonia

• Pulmonary artery erosion occasionally– Behcet’s syndrome, Rasmussen’s aneurysm in

tuberculous cavity, sleeve lobectomy

• Major systemic artery– Thoracic aortic aneurysm or graft eroding into lung– Tracheal-innominate artery fistula complicating

tracheostomy, tracheal resection

Management is Urgent

• Risk of Asphyxiation from proximal airway obstruction

• You have a potential life threatening situation • Admission to hospital is mandatory• Resuscitation in the operating room• Inform interventional radiology after life-saving

measures in the OR• Inform ICU for transfer after angiogram and

bronchial artery embolization

Five Phases of Treatment

1st phase: Emergency Room

Second phase: Operating Room

Third phase: Interventional Radiology

Fourth phase: Intensive Care Unit

Fifth phase: Interval Definitive Operation

Management in the ER: 1st phase

1. See patient immediately2. Evaluate patient quickly – administer supplemental

oxygen, secure intravenous access, rapid clinical assessment with patient sitting upright

3. Ask for CXR quickly – may give clue to side of bleeding, and then turn patient with bleeding lung side down to protect uninvolved lung from aspiration of blood

4. Obtain immediately: CBC, serum electrolytes, arterial blood gas analysis, PTT and INR, EKG, type and x-cross match blood, and consent for OR

5. Organize urgent OR and inform interventional radiology for urgent angiogram and possible embolization

Management in the OR: 2nd phase

• Secure patency of proximal airway and protect against threat of asphyxiation by rigid bronchoscopy

• Implement endobronchial measures – cold saline or dilute epinephrine solution irrigation to arrest bleeding temporarily

• Separate two lungs with double lumen tube to protect the good lung from aspiration of blood

• Interventional radiology for bronchial artery angiogram for embolization of abnormal artery; may need to look for non-bronchial collaterals to embolize as well

Remove threat of asphyxiation quickly

Only by Rigid Bronchoscopy

Rigid Bronchoscopy is necessaryto restore patency of the airway

Advantages of Rigid Bronchoscopy

• Visualize - good optics• Suction - large channel • Ventilate - resembles endotracheal tube

“ A situation where the margin between life and death is narrow, it will save the patient’s life

Bronchoscopy is the key to successful management

• Rigid bronchoscopy performed first– Ventilate patient easily– Suction effectively to remove obstructing blood clots

and restore oxygenation– Good optics to visualize and determine SIDE of

bleeding “Lateralization”– Implement endobronchial control measures to protect

good lung and to arrest bleeding: cold saline and dilute epinephrine solution irrigation

• Flexible bronchoscopy after rigid bronchoscopy to determine SITE of bleeding and possible cause - “Localization”

• Lung separation with double lumen tube to protect good lung and then come out of the OR

General Principles of TreatmentEarly Bronchoscopy

• Clear the Airway

• Secure the Airway

• Separate the Two Lungs

• Handle the Cause

Endobronchial Control MeasuresEmergency Bronchoscopy Tray

• Rigid bronchoscope• Flexible bronchoscope• Cold N/S – 4ºC• Bronchial Blocker and

Double Lumen Tube• Dilute epinephrine

solution – 200mcg in 500mls N/S

• Oxygen saturation monitor

Lung Separation Single Tube and Bronchial Blocker

Blocker in the Left Lung

Lung SeparationDouble Lumen Tube

Lung SeparationUncut Single ETT

Interventional Radiology: 3rd phase

• Important component of optimal medical treatment• Safe after patient has been stabilized in OR and the two

lungs have been separated• Thoracic aortogram and subclavian arteriogram• Search and embolize abnormal bronchial (aorta) and

non-bronchial collateral arteries (intercostal, branches of subclavian artery)

• Embolization stops bleeding and permits safe semi-urgent pulmonary resection with low operative mortality

• Resect diseased portion of lung - after bleeding has stopped and patient has made functional recovery

• Complication of embolization: spinal cord ischemia

Result of Embolization

• Remy in France• Recanalization leads to recurrent hemorrhage in

< 4months• Bleeding stopped immediately in 41/49 patients• Recurrence of bleeding in 6/41patients within 2

to 7 months• In poor surgical risk patient – embolization is the

only real solution and becomes definitive treatment

Bronchial A-V malformation and abnormal internal elastic lamina

Aspergilloma in an old tuberculous cavity

Segmental Pulmonary Artery Aneurysm

Bronchiectasis LLL and RML

Aortic graftPulmonary Fistula

Management in the ICU: 4th phase

• Patient is transferred to the ICU from the Radiology Department or the OR for close monitoring and assisted ventilation

• Plan for extubation after bleeding has subsided for 24 hours

Interval definitive treatment:5th phase

• Time is required for full recovery of lung function and thorough assessment of cardiopulmonary reserve

• Plan for definitive elective or semi-urgent operation for pulmonary resection in surgical patients with lung lesion with acceptable low operative mortality <3% when risk for re-bleeding is high

Spontaneous Pneumothorax

Spontaneous Pneumothorax

Definition: Any pneumothorax occurring in the absence of trauma (needle aspiration biopsy, needle thoracentesis, rib fractures, ruptured esophagus) may be described as spontaneous

Classification of Spontaneous Pneumothorax:1. Primary2. Secondary

Sub-classification into:• Simple• Complicated

• Tension or valvular pneumothorax• Associated bleeding – hemopneumothorax

Spontaneous Pneumothorax

Simple Tension

Complicated Spontaneous Hemopneumothorax

Spontaneous Pneumothorax1. PRIMARY TYPE

Absence of clinical evidence of pre-existing respiratory disease

• Rupture of a Local Defect usually near the lung apex– small bulla >1cm– bleb <1cm (a

localized collection of air within the visceral pleura from ruptured distended alveolus)

2. SECONDARY TYPE

Indicates presence of a clinically recognizable coexisting structural or functional parenchymal abnormality in the lung

• Rupture from an underlying diffuse lung parenchymal disease

• Most common is emphysema

Secondary Spontaneous Pneumothorax

• Commonest cause is pulmonary emphysema• Others are

1. asthma2. interstitial lung disease3. cystic fibrosis4. active tuberculosis5. histiocytosis X6. pulmonary metastases from sarcoma7. lymphangioleiomyomatosis (LAM)8. Birt-Hogg-Dube syndrome9. catamenial (related to menstruation)

Primary Spontaneous Pneumothorax

• CAUSE: an emphysematous bulla or a bleb ruptures and air leaks into the pleural cavity

• AGE incidence: young adults are especially liable• CLINICAL POINTERS: 1. sudden onset 2. unilateral pleuritic chest pain; mild dyspnea 3. diminished breath sounds over the affected

lung 4. dry cough is usually but not always present• INVESTIGATIONS: Chest x-ray on inspiration and

expiration confirms diagnosis; sometimes CT scan needed

Diagnosis

• CXR taken in full inspiration and expiration

• EKG and serum cardiac enzymes to rule out acute coronary syndrome in age >40 years

• Chest CT scan if in doubt

Simple Spontaneous pneumothorax

• SIMPLE, UNCOMPLICATED

1. Observation - depends on the degree of lung collapse and assuming that the air leak from the lung surface has sealed immediately, and it is small in size < 20% the rate of re-expansion of the lung is 1.25% per day: 10% lung collapse will resolve in 8 days and 20% in 16 days

2. Intercostal chest tube drainage if large in size >30% for about 72 hrs

• COMPLICATED Treatment is different

1. Tension type: urgent needle decompression and chest tube insertion in 2nd intercostal space in midclavicular line2. Recurrence affecting the same lung is 20% to 30% after 1st episode; 50% after 2nd episode; 80% after 3rd episode(surgical)3. Sepsis (empyema), trapped lung (surgical)4. Associated hemothorax (surgical)

Management of Spontaneous Pneumothorax

Treat by Observation only

• FIRST EPISODE

• Without associated complications of Tension Quality, Bleeding – Hemothorax, or Infection – Empyema

• Patient is stable and reliable• Degree of lung collapse is small <20%• Assuming that the air leak has sealed immediately

the rate of re-expansion of the lung is 1.25% per day: 10% lung collapse will resolve in 8 days and 20% in 16 days

be aware: Small unpredictable risk of becoming tension type

Complicated Spontaneous Pneumothorax

1. Tension or valvular type in any closed pneumothorax

life-threatening situation demanding urgent care

2. Bleeding – hemothorax

demands drainage and chest operation

Tension or Valvular Pneumothorax

• Cause1. any simple closed pneumothorax has the

potential to become tension under the right circumstances

2. communication between the lungs and the pleural cavity allows unidirectional passage of air and transmission of positive airway pressure into pleural cavity but not out of it allows considerable tension to be built up inside the pleural cavity

• Precipitating factors 1. valve action at the site of air leak persists 2. severe coughing generates positive airway pressure 3. assisted ventilation with positive airway pressure

1. Life-threatening situations in Spontaneous Pneumothorax – Tension or Valvular Type

• Clinical pointers1. sudden onset2. severe unilateral chest pain worse on breathing3. increasing respiratory distress, hypoxia and tachycardia are early signs4. cyanosis (not always present), hypotension, distended neck veins, and tracheal deviation

are late signs of a tension pneumothorax5. increased resonance and absent or diminished breath sounds on affected side of chest (hyperinflated)6. evidence of contralateral mediastinal shift

Diagnosis, Treatment

• SIMPLE SPONTANEOUS PNEUMOTHORAX– CXR taken in full inspiration and expiration– EKG and serum cardiac enzymes to rule out acute

coronary syndrome in age >40 years– Chest CT scan if in doubt

• TENSION PNEUMOTHORAX– Do not waste time– Do not do CXR or CT scan– Clinical diagnosis and immediate treatment – needle

decompression in 2nd ICS and then chest tube insertion

Spontaneous Hemopneumothorax

• Due to rupture of systemic blood vessels between 2 and 3 mm size in the vascularized intrapleural adhesions which tear as the lung collapses

• Blood loss can be substantial

2. Life-threatening situations in Spontaneous Pneumothorax – Associated Hemothorax

• Clinical pointers1. sudden onset2. severe unilateral chest pain worse on breathing3. increasing respiratory distress, hypoxia and tachycardia are early signs4. Pallor and low Hb 5. postural hypotension, collapsed neck veins6. dullness to percussion in the lower chest and absent or diminished breath sounds on affected side of chest

Treatment for Spontaneous Hemopneumothorax

• FIRST EPISODE• Operation is necessary

– Resuscitate– Intercostal chest tube drainage– Surgical chest exploration for evacuation of

blood clots, surgical hemostasis, and apical bullectomy, pleural symphysis by abrasion (not pleurectomy) of parietal pleura

Indications for chest tube insertion in Pneumothorax

• Large size at initial presentation• Increasing size• Symptomatic• Associated hemothorax• Undergoing general anesthesia• Bilateral• Tension quality• Contralateral

Indication for Surgery

• First episode with prolonged air leak > 3 days• 2nd or 3rd recurrence on same side• 1st occurrence on contra-lateral side• Associated hemothorax >1000mls• Associated pleural sepsis• Incomplete re-expansion• Occupational risks - air pilot, scuba diver, work at high

altitude• Synchronous bilateral• Life-threatening episode of tension pneumothorax - if

access to immediate care is unavailable• Patient living in remote areas

Therapeutic Options

• Apical bullectomy and parietal pleurectomy in all young adults– Video-assisted thoracoscopic approach– Limited thoracotomy

• Chemical pleurodesis in elderly patients with serious co-morbid illnesses or severe COPD– Talc– Tetracycline

Dysphagia

Clinical Presentation• An elderly 75y old man• Intermittent cervical dysphagia for 3y• Gurgling noises in the neck on drinking liquids• Occasional regurgitation of undigested food

eaten hours earlier• Foul breath• Intermittent left neck swelling• Spells of choking on swallowing• One episode of pneumonia due to choking

What is the diagnosis on barium swallow?

• What are the complications of this condition?

• Is treatment necessary?

• What treatment is possible ?

Zenker’s Diverticulum

• Most common esophageal diverticulum

• “Pulsion” diverticulum containing mucosa and submucosa

• Develops at the Pharyngo-esophageal junction in the neck

• Just above the UES (cricopharyngeus muscle) through Killian’s triangle

Develops on posterior wall of pharynx between upper and lower divisions of inferior constrictor

muscle

UES

Zenker’s Diverticulum

• Acquired – 80% occur in age >50 yrs

• Pathophysiology:– Develops because the

UES does not relax in coordination with pharyngeal contraction

Treatment is necessary and it requires an operation

• To prevent life-threatening complications due to recurrent acute aspiration pneumonia, lung abscess and empyema

• For symptomatic relief

Treatment for Zenker’s Diverticulum

• OPERATION IS NECESSARY• There is no medical treatment• Surgical treatment is curative

Always perform Cricopharyngeal Myotomy

For the diverticulum– Small < 3cm size leave it alone– Large > 3 cm size add diverticulectomy

Clinical Presentation

• A 35y old man• With a Triad - slowly worsening difficulty

swallowing, regurgitation, and some weight loss over 18 months

• Past medical history is unremarkable– No caustic ingestion– No GERD, Ulcer dyspepsia– No previous esophageal or stomach operation

What is the diagnosis on barium study?

1. What is necessary to confirm diagnosis?

2. What treatment would you recommend?

Esophageal Manometry confirms Diagnosis of Achalasia

LES does not relax during swallow Absence of peristalsis

Achalasia is a neurogenic esophageal motility disorder

• Characterized by 3 manometric findings

1. Absence of peristalsis in the body of the esophagus

2. Failure of LES to relax during swallowing - relaxation is absent or incomplete

3. Higher than normal resting LES pressure

Achalasia

What is the Cause?• North America

– cause is unknown, viral infection, autoimmune

• South America

– Chagas’ disease due to parasite Trypanosoma Cruzi

• Finding: degeneration of ganglion cells in Auerbach’s plexus

Clinical Presentation– Dysphagia for both

solids and liquids; worse with liquids

– Retrosternal burning discomfort due to food stasis and retention esophagitis

– Nocturnal regurgitation of food and choking episodes aspiration

Achalasia: Investigations and Results

BARIUM SWALLOW APPEARANCE IS CHARACTERISTIC

Esophageal dilatation

Spastic non-peristaltic contractions

Retention of contrast above poorly relaxing LES at G-E junction

‘bird’s beak’ with obstruction UGI ENDOSCOPY IS NECESSARY TO RULE OUT CANCER (PSEUDOACHALASIA) AND PEPTIC STRICTURE

Evidence of stasis

Dilated esophagus with retained food, liquid, saliva

Mucosal inflammation ‘retention esophagitis’

ESOPHAGEAL MANOMETRY IS NECESSARY TO CONFIRM THE DIAGNOSIS

Incomplete or absent relaxation of LES

Absence of normal peristalsis in body of esophagus

Treatment for Achalasia – chronic condition, no cure for it

• Aim of Treatment: relieve distal esophageal functional obstruction (LES does not relax during swallowing)

• Choices of treatment:

1.Pneumatic “Balloon” dilatation of LES, success rate of 80% decreases to 50% at 10 years; esophageal perforation risk of 5%

2.Intra-sphincteric injection of Botox, symptomatic relief of 60% decreases to 30% at 2.5 years

3.Treatment of choice is Distal esophagomyotomy and partial fundoplication effective in 90%, late problem of Postop GERD is about 15% over time

Distal Esophago-Myotomy and Partial Fundoplication

Distal Esophageal Spasm (DES)

• Clinical: severe, intermittent anterior chest pain (confused with angina), dysphagia, and presence of esophageal diverticulae

• Defined by Esophageal Manometry

1. Simultaneous contraction waves in the body of esophagus in >20% of the swallows

2. Prolonged contractions in the distal esophagus (>6 sec)

3. Frequently presence of high pressure amplitudes in the distal esophagus

4. LES abnormal – incomplete relaxation

DES

• “The lower part of the esophagus (smooth muscle portion) of patients with diffuse esophageal spasm is simultaneously and firmly contracted for an abnormally long time”

• Clinical Presentation

Severe spontaneous chest pain, intermittent dysphagia, and presence of esophageal diverticulae on barium swallow

• Differential Diagnosis

Angina pectoris

Psychoneurosis

Distal Esophageal Spasm

Corkscrew Esophagus

Treatment of DES

• Reassurance in most cases– heart disease ruled out by cardiologist– Not dealing with life-threatening condition– Medical Therapy with nitrates, calcium channel

blockers, antireflux measures• Surgical treatment cannot correct the functional disorder

Long Esophagomyotomy to lower amplitude of waves and resting pressure; add Partial Fundoplication– Performed in selected refractory cases– Successful symptomatic relief in 50% to 65%

Nutcracker Esophagus

• Manometric Findings

• High Amplitude, Peristaltic Esophageal Contractions

• > 180 mmHg amplitude• Long duration

contractions > 6 sec

• LES is normal

Treatment

• Reassurance in most cases

• Must exclude myocardial ischemia

• Long Esophagomyotomy in selected cases; add Partial Fundoplication

Pathologic Gastroesophageal Reflux Disorder

Definition• Frequent retrograde flow

of gastric contents across the GE junction into the esophagus

Pathophysiology• Incompetent LES• Loss of barrier function of

the LES, either continuous or intermittent

REFLUXATE

– Acid or Alkaline reflux

HCL

Pepsin

Bile acids

Bile salts

What are the normal properties of LES?

• Major barrier to reflux – HIGH PRESSURE ZONE• Physiological sphincter• Located in the distal 2 to 4 cm of esophagus• Normal resting tone 15 to 30 mm. Hg• Relaxation is coordinated with primary peristalsis

• LES pressure is decreased by estrogen, progesterone, nitroglycerine, calcium channel blocker, cigarette smoking, alcohol, fat rich meals, gastric distension,

coffee, chocolates, vagotomy, distal esophagomyotomy

Incompetent Lower Esophageal Sphincter causes GERD

• WHAT ARE THE CAUSES OF PATHOLOGIC GERD?

• Idiopathic - majority• After pneumatic dilatation

or esophagomyotomy for Achalasia

• Scleroderma• Large fixed hiatus hernia• Gastric outlet obstruction• Prolonged nasogastric

tube insertion

• WHAT ARE THE TYPICAL SYMPTOMS?

• Unpleasant and intense substernal burning sensation

• Substernal chest pain• Postural and/or

postprandial regurgitation• Water brash• Flatulence• Intermittent difficulty with

swallowing

Complications of Pathologic Gastroesophageal Reflux Disorder

1. ESOPHAGUSreflux esophagitis: inflammation, erosion, ulceration, fibrosis and peptic stricture

chronic blood loss and iron deficiency anemia,

Barrett’s epithelium and risk of adenocarcinoma

2. UES SPASM Zenker’s diverticulum

3. MOUTH teeth decay and loss of enamel

4. PROXIMAL AIRWAY laryngitis, wheezing, cough

5. LUNGS aspiration pneumonia lung abscess, pulmonary fibrosis, bronchiectasis, empyema

Reflux and Esophageal Damage

How is the diagnosis of GERD made?• Barium swallow and UGI series

– radiologic reflux, hiatus hernia, esophageal stricture, aspiration, spasm in UES

• Upper GI endoscopy– esophagitis (erythema, erosions, ulcerations, stricture

formation), columnar-lined esophagus • Esophageal manometry

– decreased LES, ineffective esophageal peristalsis• 24-hour esophageal pH monitoring

– Most sensitive test for acid reflux: number of reflux episodes, duration of reflux, upright vs. supine

• 24-hour impedance pH study detects number of reflux episodes and whether acid or alkaline reflux

What is the treatment for GERD?

1. Always consider medical treatment first

• Dietary modification– Small meals, avoid

eating for 2 hrs before going to bed

• Elevate head of the bed• Abstain from coffee,

alcohol, trigger foods• Drugs: Antacids, PPI, H2-

blockers

2. Surgical therapy requires fundoplication

• When GERD is refractory to optimal medical therapy given for a minimum of 6 months

• When GERD is associated with complications of hiatus hernia, complications in the airway – recurrent aspiration, asthma like symptoms, laryngitis

An elderly patient in the ER complaining of central chest pain radiating into left shoulder, retching,

and coffee ground emesis. Barium study from 12 months ago for similar complaint is shown

1. Would you have sent her home on first visit to the ER with chest pain and MI was ruled out?

2. What condition is shown?

3. How does it affect the patient?

4. What serious problem can occur?

Complications of Hiatus Hernia

1. Incarceration strangulation ischemic perforation death

2. Anemia – chronic blood loss due to mucosal congestion

3. Dyspnea – large hernia

4. Cardiac Arrhythmias – extrinsic pressure

5. Volvulus obstruction

6. Perforation

7. Massive Bleeding

Type I

Type II

Type III

Associated GERD

Risk of Incarceration/strangulation

Combination of GERD and Incarceration

Type IV hiatus hernia - volvulus

Intrathoracic stomach with risk of volvulus, associated herniationof transverse colon, small bowel

Management of Hiatus Hernia

Classification Type I – most common

Type II – very rare

Type III – mixed Type I and II

Type IV

INCIDENCE 85% to 90% Pure is rare < 1%

About 6% Least common

SYMPTOMS May be asymptomatic or have GERD

Asymptomatic or come to ER with incarceration/strangulation

Symptoms of incarceration and reflux

Nearly whole stomach in the chest; risk of volvulus, obstruction, bleeding

INDICATION FOR OPERATION

GERD refractory to medical therapy

To prevent strangulation and ischemic perforation

Medical therapy is not that effective

Anatomical correction is indicated

A barium study is finally given to a 45y old patient whose complaint for difficulty swallowing was

ignored for 5 months

• What are the clinical features of this condition?

• What is the differential diagnosis?

• What investigations should be undertaken?

• What treatments are available?

Esophageal Cancer

• What are the two main cell types?

Adenocarcinoma

Squamous cell carcinoma

• What is the most common histology?

Worldwide: squamous cell carcinoma 95%

Western world: adenocarcinoma

Squamous Cell Cancer – what are the etiological factors?

• Strong association with excess cigarette smoking and alcohol consumption

• Three dietary factors are high intake of nitrosamines (food preservatives), low intake of both vitamin A and nicotinic acid, and chronic iron deficiency

• Long standing achalasia, accidental caustic ingestion• Tylosis palmaris et plantaris• Celiac disease

• Silica in wheat • Previous radiation therapy to the mediastinum

Adenocarcinoma – what is the cause?

• Incidence of adenocarcinoma is rising in NA,UK, Europe, Australia – an explosion

• Due to Chronic GERD – not necessarily acid reflux

• Refluxate: acid, pepsin, bile salts, bile • Develops in acquired metaplastic Barrett’s

epithelium

Chronic GERD: Adenocarcinoma

Mucosal Squamous Epithelium

Metaplasia

Mucosal Columnar Epithelium

“Barrett’s Esophagus” specialized intestinal

Dysplasia

Low grade High Grade

Adenocarcinoma

In situ Invasive

Symptomatic GERD Barrett’s Esophagus Adenocarcinoma

Barrett’s Esophagus

Esophageal Cancer

Clinical Presentation

1. Progressive dysphagia, initially for solids and later for liquids2. Progressive weight loss3. Other symptoms – chest pain, back pain, hoarseness, choking and aspiration, symptoms of metastasis

Diagnostic Tests

• Barium UGI series• Esophagoscopy and

mucosal biopsies

Tests for Staging• CT scan chest and

abdomen• Esophageal U/S and LN

biopsy• PET scan

Treatment for Esophageal Cancer

1. Surgical: esophagectomy and reconstruction with stomach or colon interposition

2. Induction chemotherapy and radiotherapy before surgery

3. Definitive Radiotherapy only: local treatment• Intent: palliation – symptom control• Intent: cure – disease control

4. Definitive chemotherapy combined with radiation5. Esophageal stent: palliation

Esophagectomy

Benign Tumors of Esophagus

• Leiomyoma is the most common• 90% occur in the lower 2/3rd of the esophagus• Grow slowly and cause dysphagia when size becomes

>5 cm• Treatment is surgical by enucleation

Esophageal Leiomyoma

Chest Trauma

Acute Cardiac Tamponade

• Immediately life-threatening chest injury

• Disturbed physiology occurs because of combination of two factors:

1. inability of the fibrous parietal pericardium to stretch in acute situation

2. rapid intrapericardial accumulation of blood

In acute situation even as little as 120 to 150 ml blood in the pericardial space can lead to acute cardiac tamponade

Acute Cardiac Tamponade

• Pathophysiology: is due to Poor Cardiac Filling– Rapid bleeding into the pericardial sac pressure on

right side of the heart impaired venous return to the heart decreased stroke volume and cardiac output (the pericardium does not stretch!)

• Clinical Features– Suggestive wound – blunt or penetrating chest injury– Pulse↑, BP↓, JVP↑ Pulsus paradoxus, Kussmaul’s

sign (Jugular venous distension with inspiration)• Define Beck’s Triad

– Hypotension, Raised JVP, Muffled heart sounds

Acute Cardiac TamponadeIntrapericardial Pressure

Hempericardium120 -150 mls

parameters

Acute Cardiac Tamponade

Diagnosis of Acute Cardiac Tamponade in Chest Trauma

1. Echocardiogram is diagnostic test

2. Nature of the chest injury

3. Not from CXR – don’t expect to see cardiomegaly

Treatment is Urgent

• Trauma Resuscitation Protocol for ABC

• Immediate IV fluid bolus• Perform needle

pericardiocentesis and follow with mandatory surgical exploration

• Pericardiocentesis is a temporizing procedure

Pericardiocentesis

Sub-xiphoid approach

Massive Hemothorax

• Immediate threat to life• How is it diagnosed?

– Pulse↑, BP↓, JVP↓, O2 ↓

– Abnormal clinical chest findings - decreased breath sounds and dullness to percussion

– Abnormal CXR, CT – Large blood loss from

chest tube: initial 1500mls 300mls/hr

Massive Hemothorax

• Pleural space can accommodate large amount of free and clotted blood >1.5L

• Hypotension from loss of circulating volume and tension effect

• Hypoxia from compressive atelectasis

Massive Hemothorax

What is the source of significant bleeding into the pleural space?

1. Low pressure bleeding from lung laceration caused by jagged, sharp ends of a fractured rib often self-limiting

2. High pressure bleeding from Intercostal artery, Internal mammary artery, Aorta, Major arch arteries, Vena Cava, Azygous vein continuous bleeding and not-self limiting

Treatment of Massive Hemothorax

URGENT TREATMENT

1.Replace blood volume lost

2.Insert chest tube and monitor for blood loss

3.Aim to evacuate blood and blood clots as much as possible

4.Use cell saver, if available

5.Consider urgent operation

When do you decide that urgent operation is indicated in Massive Hemothorax?

• Initial chest tube drainage of >1500 mls of blood

• Persistent bleeding after initial drainage: >300mls of blood loss/hr for 3 hrs

• Unevacuated residual blood and blood clots on CXR

Open Pneumothorax

• Immediately life-threatening chest injury

• Serious because it causes Acute Ventilatory Failure

• What is the medical term for a “sucking chest wound”?– Open pneumothorax

Penetrating chest injury – gun shot

Open Pneumothorax

• Diagnosis of Open Pneumothorax is obvious

• Clinical Features are:

1. open chest wound

2. with air movement through the chest wall defect

3. lung is not expanded on CXR

1. If the chest wall defect is large – 2/3rd size of tracheal lumen

the effect is very serious and immediate air preferentially passes through the defect (least

resistance) during inspiration immediate respiratory distress ACUTE

VENTILATORY FAILURE death occurs rapidly from hypoxia

2. If the chest wall defect is small the effect is less serious

and outcome will depend on vital capacity

Pathophysiology

Treatment in the ER should be Immediate

• How is open pneumothorax treated?

1. Cover the chest wall defect with sterile three-sided occlusive airtight dressing

2. Insert intercostal chest tube as soon as feasible

3. Alternate treatment is endotracheal intubation and assisted positive pressure ventilation

4. Surgical closure in OR

20y patient involved in MVA is found to be markedly hypoxic in the ER. CXR was

performed.

1. What is illustrated on CXR?

2. Why is there a change in oxygen saturation?

3. What is the reason for NGT insertion?

4. What is the management?

Pulmonary Contusion is very Serious• Interstitial & parenchymal

hemorrhage alveolar collapse

• Extravasation of blood and plasma into alveoli.

• V-Q Mismatch• Hypoxemia that is refractory

to increase in FiO2

• Decrease in pulmonary compliance and increase in work of breathing.

• Occurs in 70% of severe blunt trauma

• Mortality overall 20 – 30% Seen immediately on CXRSegmental, Lobar, Whole lung

Chest Trauma

• The most common physiologically significant injury resulting from blunt chest trauma is

a. flail chestb. pulmonary hematomac. subcutaneous emphysemad. pulmonary contusione. diaphragm rupture

Chest Trauma

• The most effective single modality in treating severe pulmonary contusion associated with post-traumatic respiratory distress and severe hypoxia is

a. fluid restrictionb. intravenous albuminc. assisted ventilation with pressure supportd. diuresise. methylprednisone

Treatment of Pulmonary Contusion

1. Restrict IV Fluids giving <1500mls/day (important)2. Antibiotic seldom indicated and only for sepsis

complicating contusion3. IV serum albumin and IV Lasix to reduce alveolar edema

(helps)4. The single most effective modality for treatment of

pulmonary contusion is mechanical ventilation with addition of PEEP– Improves FRC– Improves oxygenation by keeping alveoli open– Insert chest tube to prevent tension pneumothorax– Uncomplicated lung contusion will heal in 5 to 10 days

Flail Chest Injury

Immediately life-threatening chest injury

• Indicates that blunt chest trauma is severe

• Clinically obvious by paradoxical chest wall movement if it is anterior or lateral but not if posterior in location

• Occurs because of two separate fractures in more than 3 adjacent ribs

A. Anterior FlailB. Lateral Flail

Diagnosis of Flail Chest Injury

– Blunt chest injury with multiple rib fractures seen on CXR

– Paradoxical chest wall movement Flail Segment of chest wall sucks in with inspiration and pushes out with expiration opposite to the movement of rest of the chest wall

– Respiratory compromise (hypoxia) is not due to paradoxical respiration

TRAUMA VICTIMCHEST INJURY

BRUISING ON CHEST WALLSURGICAL EMPHYSEMA

ACUTE CHEST PAINBREATHING DIFFICULTY

In Flail Chest Injury Hypoxia is caused by combination of 4 factors

1. Damaged painful unstable chest wall (multiple rib fractures cannot breathe well and cough well retention of bronchial secretions, blood clots retention atelectasis V/Q mismatch hypoxia)

2. Underlying lung contusion (always present intra-parenchymal and alveolar bleeding plus increased capillary permeability V/Q mismatch hypoxia

3. Pleural space problems ( always hemopneumothorax compressive atelectasis V/Q mismatch hypoxia)

4. Chest wall muscle damage and spasm expansion↓

What is the cause of respiratory compromise in Flail Chest Injury?

1.Damaged painful unstable chest wall– Normal ventilatory force is lost lung expansion

decreases FRC falls– Cough is impaired retention of secretions

retention atelectasis V/Q mismatch hypoxia 2. Underlying lung contusion

– Hemorrhagic, edematous, non-compliant lung impaired diffusion hypoxia

3. Pleural space problems– Hemothorax and/or pneumothorax compressive

atelectasis V/Q mismatch hypoxia4. Chest wall muscle damage and spasm, increased work

of breathing and oxygen demand, hypoxia muscle fatigue and oxygen debt

Flail Chest Injury

Multiple rib fractures Acute chest wall pain

Lung contusion is always present Impairs gas exchange

Management of Flail Chest Injury

ISOLATED FLAIL CHEST INJURY

– Admit to ICU, supplemental oxygen, optimal pain control (best is by thoracic epidural analgesia), physiotherapy, insert chest tube if needed, bronchodilators, restrict IV fluids (worsens edema from lung contusion)

– Refractory hypoxia admit to ICU, assisted ventilation, insert chest tube (must do this, otherwise risk tension pneumothorax

FLAIL CHEST INJURY combined with MULTIPLE INJURIES

– Admit to ICU after life-threatening injuries have been looked after

– Assisted ventilation to maximize oxygenation

– Optimal pain control– Chest tube inserted on

injured side to prevent tension pneumothorax (risk of positive pressure ventilation)

Chest Trauma

• A 24-year-old man is brought into the ER after a fall from a ladder. His breathing is laboured, and he is cyanotic. He is complaining of right chest pain. There is subcutaneous emphysema on the right side. No breath sounds can be heard in the right lung field, which is hyper-resonant to percussion. Contralateral tracheal deviation is present. Among the following choices, the most appropriate next step in his management is:

a. obtaining a stat chest X-rayb. insertion of an endotracheal tubec. cricothyroidotomyd. stat arterial blood gas analysise. Immediate needle decompression and chest tube insertion

Tension Pneumothorax

• Immediate treat to life is due to combination ofHYPOXIA and HYPOTENSION

• HYPOXIA due to V/Q Mismatch– Ipsilateral lung collapse– Mediastinal shift

contralateral lung compression

• HYPOTENSION due to positive intra-thoracic pressure– Impaired venous return– Reduced stroke volume

reduced cardiac output hypotension

This is a Clinical Diagnosis

TensionPneumothorax is life-threatening

1. Progressive accumulation of air in pleural space under pressure

2. Ipsilateral lung collapse V/Q mismatch hypoxia

3. Contralateral mediastinal shift and lung compression V/Q mismatch hypoxia

4. Severe impairment of ventilation*

5. Impaired venous return ↓CO*

6. Rapid cardio-respiratory collapse

Pathophysiology of Tension Pneumothorax

Pneumothorax

TENSION SIMPLE

Pathogenesis of Tension Pneumothorax

• Any closed pneumothorax (spontaneous or traumatic) has the potential to become tension (valvular) type under the right circumstances

• One-way air leak from lung surface (ruptured bulla, lacerated lung) is always present

• Progressive accumulation of air in the pleural space under positive airway pressure (right circumstance!) until intra-thoracic pressure becomes positive – Severe coughing and straining– Endotracheal intubation and assisted ventilation

Problem Finding Emergency Treatment

Tension pneumothorax is a clinical diagnosis

May occur in simple closed pneumothorax or closed traumatic pneumothorax

Bulging hemithorax, unilateral diminished breath sounds, severe dyspnea, pleuritic chest pain, tachypnea subcutaneous emphysema, contralateral tracheal deviation shock, cyanosis, distended neck veins

Immediate decompression of pleural space by angiocath needle inserted in the 2nd intercostal space in midclavicular line

Followed by chest tube insertion and under water seal drainage

19-year-old man has presented to the ER complaining of severe difficulty breathing and left

acute chest pain after a fall off a roof.

1. What are the clinical features of this condition?

2. What is the reason for P140/min,R40/min, BP80/60, O2 sat 87%?

3. Was CXR absolutely necessary for diagnosis?

4. What is the immediate treatment?

Immediately life-threatening chest injury: Tracheal-bronchial Injuries

• Penetrating 3-8%– Usually cervical

• Blunt 0.5 – 2%– 80% occur < 2 cm. from

carina– Mechanisms:– Blunt: “dashboard” injury

in neck– Thoracic: Traction –

Rupture - Shearing

• Associated injuries are common and often the determinant of prognosis

Extensive subcutaneous emphysema due to ruptured right main bronchus

SUSPECT diagnosis and confirm by BRONCHOSCOPY

Chest Injury

• High speed MVA• Blunt chest injury on

left side with lower rib fractures

• Bleeding in the peritoneal cavity

• Pelvic fracture• What is the injury in

the chest on CXR?

Ruptured left hemidiaphragm and hemothorax with contralateral mediastinal shift

Thoracic Aortic Injury

Rib Fracture

• A single rib fracture in patient with pre-existing compromised lung function may precipitate respiratory failure

Chest Trauma

• A 55 year old man involved in a car accident has been placed on assisted ventilation because of severe head injury. He was noted to have bruising and surgical emphysema on the right lateral chest wall but no pneumothorax. The ventilator setting is rate 16/min, tidal volume 500 mls, FIO2 of 40%, and PEEP of 10 cm of water pressure. He develops sudden tachycardia, hypotension, increase in airway pressure, and hypoxia. The most likely cause is

a. open pneumothoraxb. systemic air embolismc. cardiac tamponaded. tension pneumothoraxe. myocardial contusion

Management of Traumatic Closed Pneumothorax

• Indications for chest tube insertion– When large pneumothorax present is compromising

lung function– When small pneumothorax and/or surgical

emphysema present in patient requiring general anesthesia – to prevent tension pneumothorax

– When hemo pneumothorax present – Patient placed on assisted ventilation in the OR or in

ICU

• Size of chest tube needed in trauma– Large bore 28F or 32F

Single or Multiple Rib Fractures in Blunt Chest Injury

• Expect damage to extra-thoracic soft tissue and muscles, laceration of intercostal vessels and nerves

• Suspect associated underlying lung injury – contusion or laceration

• Acute chest wall pain prevents deep breathing and effective coughing resulting in retention of bronchial secretions with consequent atelectasis and finally Hypoxia due to V/Q mismatch worsening respiratory distress and infected atelectasis

• Beware of associated complications of rib fractures• Pneumothorax• Hemothorax• Associated injuries in the chest and abdomen

Optimal Management of Fractured Ribs

Out-patient Treatment

– Reliable patient without pre-existing lung disease with 1 to 3 fractured ribs without pneumothorax, hemothorax and hypoxia

– Able to breathe well and cough well

– Effective relief of acute chest wall pain for 3 weeks is necessary – NSAIDS, Oral Narcotics, intercostal Nerve Blocks

In-patient Treatment– > 3 fractured ribs with or

without associated complications of pneumothorax or hemothorax, requiring supplemental oxygen

– Need effective control of pain with IV narcotics or epidural analgesia, physiotherapy, tracheal suctioning and bronchodilators

– May need intercostal chest tube drainage

Rib Fracture

• A single rib fracture in patient with pre-existing compromised lung function may precipitate respiratory failure

• Multiple rib fractures >3 # admit to hospital for minimum of 72 hours – adequate pain control, monitor for complications in the chest – hemothorax, pneumothorax

• Effective pain control for minimum of 3 weeks clinical assessment and repeat CXRs

Chest Injury and Acute Chest Wall Pain

• Demands immediate and optimal pain relief• Must restore ability to breathe well and cough well to

protect the lungs against retention atelectasis V/Q mismatch and hypoxia

• Use– Oral opiods and NSAIDS – Intercostal nerve blocks– Epidural analgesia – most effective

• Watch out for respiratory depression– if opiods used in hypoxic patient